Pagala M K, Sandow A
J Pharmacol Exp Ther. 1976 May;197(2):439-51.
This report extends earlier research, done with external media at pH 7.2, to new studies at pH 6.4 and 8.4 as well as 7.2, to determine the roles of the protonated and neutral forms of physostigmine (a weak base with pKalpha = 8.2) in causing twitch potentiation of the frog sartorius muscle. Physostigmine, especially at relatively high pH (8.4) and concentration (1.5 mM), considerably blocks excitation. However, the results show in general that physostigmine potentiation increased peak contraction time and thereby indicate that potentiation is occurring in terms of prolongation of the active state. At pH 6.4 and 8.4, 1 mM physostigmine causes no change in the mechanical threshold of K depolarization contractures of toe muscles, as found previously at pH 7.2. Physostigmine increasingly prolongs the action potential as pH rises, i.e., in positive correlation with the twitch potentiation, thus indicating that this electrical change is the prime determinant of the potentiation.
本报告将早期在pH 7.2条件下与外部介质进行的研究扩展至在pH 6.4、8.4以及7.2条件下开展的新研究，以确定毒扁豆碱（一种pKα = 8.2的弱碱）的质子化形式和中性形式在引起青蛙缝匠肌抽搐增强方面所起的作用。毒扁豆碱，尤其是在相对较高的pH（8.4）和浓度（1.5 mM）下，会显著阻断兴奋。然而，结果总体表明毒扁豆碱增强作用会增加峰值收缩时间，从而表明增强作用是通过延长激活状态而发生的。在pH 6.4和8.4条件下，1 mM毒扁豆碱不会导致趾肌K去极化挛缩的机械阈值发生变化，这与之前在pH 7.2条件下的发现一致。随着pH升高，毒扁豆碱会越来越多地延长动作电位，即与抽搐增强呈正相关，因此表明这种电变化是增强作用的主要决定因素。
